期刊
CELL METABOLISM
卷 27, 期 3, 页码 667-+出版社
CELL PRESS
DOI: 10.1016/j.cmet.2018.02.001
关键词
-
资金
- Intramural Research Program of the NIA/NIH
- KRIBB Research Initiative Program (Korean Biomedical Scientist Fellowship Program), Korea Research Institute of Bioscience and Biotechnology, Republic of Korea
- Paul F. Glenn Foundation for Medical Research
- NIH/NIA MERIT award [R01 AG028730]
The role in longevity and healthspan of nicotinamide (NAM), the physiological precursor of NAD(+), is elusive. Here, we report that chronic NAM supplementation improves healthspan measures in mice without extending lifespan. Untargeted metabolite profiling of the liver and metabolic flux analysis of liver-derived cells revealed NAM-mediated improvement in glucose homeostasis in mice on a high-fat diet (HFD) that was associated with reduced hepatic steatosis and inflammation concomitant with increased glycogen deposition and flux through the pentose phosphate and glycolytic pathways. Targeted NAD metabolome analysis in liver revealed depressed expression of NAM salvage in NAM-treated mice, an effect counteracted by higher expression of de novo NAD biosynthetic enzymes. Although neither hepatic NAD(+) nor NADP(+) was boosted by NAM, acetylation of some SIRT1 targets was enhanced by NAM supplementation in a diet-and NAM dose-dependent manner. Collectively, our results show health improvement in NAM-supplemented HFD-fed mice in the absence of survival effects.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据